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抗结核药物所致肝损害(anti-TB drug-induced hepatotoxicity,ATDH)是结核病治疗过程中备受关注的问题。ATDH风险不仅未得到有效控制,且呈日益加重的趋势[1]。ATDH的致病机制可能源自药物或其代谢产物的作用,也可能源自免疫介导的药物应答反应等[2]。很多情况下,导致肝损害的确切机制和因素仍不得而知。一些环境危险因素(如年龄、性别、肝脏疾病、营养状态、酒精摄入量、乙肝、丙肝或HIV感染等)与ATDH易感性有关[3],遗传因素也可能影响ATDH易感性[4]。抗结核药物经各种酶代谢生成毒性较低的产物,而这些酶的基因多态性很可能是影
Anti-TB drug-induced hepatotoxicity (ATDH) is an issue of great concern in the treatment of tuberculosis. ATDH risk not only failed to be effectively controlled, and the growing trend [1]. The pathogenesis of ATDH may result from the drug or its metabolites, may also be derived from immune-mediated drug response [2]. In many cases, the exact mechanism and factors leading to liver damage remain unknown. Some environmental risk factors (such as age, gender, liver disease, nutritional status, alcohol intake, hepatitis B, hepatitis C or HIV infection) are associated with ATDH susceptibility [3] and genetic factors may also affect ATDH susceptibility [4]. Antituberculosis drugs are metabolized by a variety of enzymes to produce less toxic products, and the genetic polymorphisms of these enzymes is likely to be the shadow